home study (health outcomes and measures of the environment study)

Conditions: Environmental Exposures; Child Development; Lead and Injury Reduction

Summary: the goal of the home study is to quantify the impact of low-level fetal and early childhood exposures to environmental toxicants including lead, mercury, and other metals, pesticides, polychlorinated biphenyls (pcbs), persistent organic pollutants (pbdes/pfcs), phthalates, phenols, environmental tobacco smoke, and alcohol on child development, neurobehavior, health, and growth. the home study will also evaluate meconium as a biomarker for fetal exposure and test the effectiveness of home repairs to control lead hazards and injuries in early childhood.

this study aims to examine the effects of low-level exposures to prevalent neurotoxicants on health, growth, and neurobehavior among a representative sample of children. pregnant women were enrolled in the project around 16 weeks of gestation. in the first phase of the study, we followed children resulting from the pregnancy through the age of 36 months. the second phase extended follow-up through 72 months. phase 3 extended follow-up to 8 years (range 7.5-10) with comprehensive neurobehavioral assessments. phase 4 will allow follow-up at 12 years (range 11-13), and includes measures of health, growth and body composition, behavior and mental health, and neuroimaging. to address the potential adverse health risks of environmental chemicals, including persistent pollutants such as pbdes and pfcs and other non-persistent chemicals, on fetal, infant, and child neurobehavior, the investigators are systematically examining their associations with endocrine function, cognition, learning and memory, motor skills, attention and executive function, and behavior from age 1 to 7.5-10 years. the investigators are also examining exposures at different developmental stages (in utero at 16 weeks of gestation, early childhood, school age, preadolescence) using stored biological samples and measure child neurobehavior at 1, 2, 3, 4, 5, 8, and 12 years. this longitudinal study will allow the investigators to determine the dose response, windows of susceptibility, and persistence of the association. the investigators are also examining the contribution of pbde exposures from house dust in a subset of children who have complete sets of samples of maternal serum and child serum collected from annual visits along with extensive measures of mouthing behaviors. hypotheses from the four phases of the study are as follows: 1. in utero exposures measured by survey (alcohol and ets), maternal and cord blood (lead and mercury) maternal and cord serum (ets), and urine (pesticides) are less predictive of in utero effects of prevalent toxicants, including cognition, behavior problems, and growth compared with the same toxicants in meconium. 2. prenatal and postnatal exposures to prevalent pesticides and ets are associated with adverse neurobehavioral effects, and growth delay in children. 3. higher lead exposure, measured during pregnancy and early childhood using maternal blood, cord blood, meconium and children's blood, will be associated with lower iq scores and more behavioral problems for children with a maximal blood lead level \< 5 mg/dl. 4. children in the lead treatment arm will have: blood lead that is 2.7 mg/dl lower, higher iq scores, greater growth velocity, and fewer behavioral problems than children in the control group. 5. levels of lead in dust, soil and water will be significantly lower for housing units in the lead treatment arm compared with the injury control arm at 36 and 48 month home visits. 6. a multifactorial, housing intervention will reduce residential injury by 30 percent among children in the injury treatment arm compared with those in the lead treatment arm. 7. prenatal and postnatal exposures to pbdes and pfcs are associated with altered thyroid hormone levels and deficits in infant and child neurobehavior 8. with increasing child age, pbde exposure from household dust becomes a stronger predictor of child serum pbde concentration than exposure from placenta or breast milk. 9. developmental pbde and pfc exposures are associated with internalizing symptoms. 10. developmental pbde and pfc exposures are associated with adverse changes in anatomical structure, neurochemistry, organization of white matter tracts, and connectivity of neural networks. 11. pfas affect the gene expression and function of several biological pathways that program the fetus/infant towards a 'thrifty phenotype'. this leads to accelerated early childhood growth, increased fat mass, and features of metabolic syndrome.

Eligibility criteria:
inclusion criteria: * pregnancy * participating prenatal practice/clinic * participating hospital exclusion criteria: * residence outside study area * plans to move outside study area within 1 year * home built after 1978 * less than 18 years of age * beyond 19 weeks of gestation * diagnosis of diabetes * diagnosis of seizure disorder (taking anti-seizure medication) * diagnosis of thyroid disorder * diagnosis of aids or positive hiv test * diagnosis of bipolar disorder * diagnosis of schizophrenia * diagnosis of cancer resulting in radiation treatment or chemotherapy

Keywords: home environmental exposure neurobehavior child development lead exposure child injury adolescence adiposity neuroimaging